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The Scientific World Journal
Volume 2013, Article ID 536350, 10 pages
Research Article

Involvement of MAPKs and PLC Pathways in Modulation of Pacemaking Activity by So-Cheong-Ryong-Tang in Interstitial Cells of Cajal from Murine Small Intestine

1Department of Sasang Constitutional Medicine, College of Korean Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea
2Division of Longevity and Biofunctional Medicine, Pusan National University School of Korean Medicine, Beomeori, Mulgeum-eup, Yangsan, Gyeongsangnam-do 626-870, Republic of Korea

Received 7 August 2013; Accepted 5 September 2013

Academic Editors: A. Beltsis, M. Klüppel, and C. Rizzetto

Copyright © 2013 Min Woo Hwang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Purpose. Interstitial cells of Cajal (ICCs) are the pacemaker cells that generate slow waves in the gastrointestinal (GI) tract. We have aimed to investigate the effects of Socheongryong-Tang (SCRT) in ICCs from mouse’s small intestine. Methods. The whole-cell patch-clamp configuration was used to record membrane potentials from cultured ICCs. Intracellular Ca2+ ( ) increase was studied in cultured ICCs using fura-2 AM. Results. ICCs generated pacemaker potentials in mouse’s small intestine. SCRT produced membrane depolarization in current clamp mode. Y25130 (5-HT3 receptor antagonist) and RS39604 (5-HT4 receptor antagonist) blocked SCRT-induced membrane depolarizations, whereas SB269970 (5-HT7 receptor antagonist) did not. When GDP-β-S (1 mM) was in the pipette solution, SCRT did not induce the membrane depolarizations. analysis showed that SCRT increased . In the presence of PD98059 (p42/44 MAPK inhibitor), SCRT did not produce membrane depolarizations. In addition, SB203580 (p38 MAPK inhibitor) and JNK inhibitors blocked the depolarizations by SCRT in pacemaker potentials. Furthermore, the membrane depolarizations by SCRT were not inhibited by U-73122, an active phospholipase C (PLC) inhibitor, but by U-73343, an inactive PLC inhibitor. Conclusion. These results suggest that SCRT might affect GI motility by the modulation of pacemaker activity through MAPKs and PLC pathways in the ICCs.